title: SIRT3 controls cancer metabolic reprogramming by regulating ROS and HIF.
abstract: In this issue of Cancer Cell, Finley and coworkers report that the genetic loss of the deacetylase SIRT3 leads to metabolic reprogramming toward glycolysis. This shift is mediated by an increase in cellular reactive oxygen species (ROS) generation that amplifies HIF-α stabilization and HIF-dependent gene expression, thereby driving the tumor phenotype.
authors.affiliation: Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E. Superior St. Searle Bldg. 4-685, Chicago, IL 60611, USA. p-schumacker@northwestern.edu
authors.forename: Paul T
authors.initials: PT
authors.lastname: Schumacker
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism*; D055432:Metabolomics / Q000379:methods; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D056566:Sirtuin 3 / Q000235:genetics / Q000378:metabolism*
chemical_list: D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D017382:Reactive Oxygen Species; C466093:SIRT3 protein, human; D056566:Sirtuin 3; D005947:Glucose